The molecular basis for the responses of neural stem cells (NSCs) to injury and chronic neuroinflammation are unknown. In mouse models of multiple sclerosis, chronic neuroinflammation have deleterious effects in NSCs (Imitola et al, 2011) by decreasing their self-renewal capacity.
Our goal is to identify and validate genes that mediate the responses of neural stem cells (NSCs) to CNS injury in multiple sclerosis and brain cancer in the so-called injury-induced stem cell niches.
Few candidate genes have been validated for NSCs function in CNS pathology such as the chemokine receptor CXCR4 that mediates the migration of human NSCs to sites of Injury and brain tumors (Imitola et al, 2004). We hope to translate novel molecular targets on NSCs to enhance human CNS repair and regeneration.
1. Inflammation transcriptional control of NSCs and brain cancer stem cell intrinsic properties.
2. Modeling inflammation-induced neurodegeneration and repair with iPSCs
iPSCs, cell culture, isolation of neural stem cells from multiple sclerosis models, confocal microscopy, organotypical slices, RNA isolation and gene expression analysis with computational biology tools.